Professional Documents
Culture Documents
Saudi Diploma in Family Medicine Center of Post Graduate Studies in Family Medicine
Presented by: Dr. Zekeriya Aktrk zekeriya.akturk@gmail.com www.aile.net
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Cardiovascular diseases (CVD) are the main cause of morbidity and mortality among the Saudi population1 A significant proportion of hospital admissions is due to CVD, whether acute or chronic or to cardiac procedures including angiograms2
1-Al Balla SR,. J Trop Med Hyg 1993;96:157-62 2-Bamgboye EA, Saudi Med J 1993;13(1):8-13. ] .
Hyperlipidemia
Michele Ritter, M.D. Argy Resident February, 2007
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Atherosclerosis
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Causes of Hyperlipidemia
Diet Hypothyroidism Nephrotic syndrome Anorexia nervosa Obstructive liver disease Obesity Diabetes mellitus Pregnancy Obstructive liver disease Acute heaptitis Systemic lupus erythematousus AIDS (protease inhibitors)
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Polyunsaturated
Saturated
Trans
Raises LDL
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Dysbetalipoproteinemia
Affects 1 in 10,000 Results in apo E2, a binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL) Increased risk for atherosclerosis, peripheral vascular disease Tuberous xanthomas, striae palmaris
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Checking lipids
Nonfasting lipid panel
measures HDL and total cholesterol
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HDL
< 40 Low 60 High
Serum Triglycerides
< 150 normal 150-199 Borderline 200-499 High 500 Very High
Total Cholesterol
< 200 Desirable 200-239 Borderline 240 High
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LDL Goals
0-1 Risk Factors:
LDL goal is 160 If LDL 160: Initiate TLC (therapeutic lifestyle changes) If LDL 190: Initiate pharmaceutical treatment
2 + Risk Factors
LDL goal is 130 If LDL 130: Initiate TLC If LDL 160: Initiate pharmaceutical treatment
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Treatment of Hyperlipidemia
Lifestyle modification
Low-cholesterol diet Exercise
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Agents
Lovastatin Pravastatin Ezetimibe
Effects (% change)
LDL (18-55), HDL (5-15) Triglycerides (7-30) LDL( 14-18), HDL (1-3) Triglyceride (2) LDL (15-30), HDL (15-35) Triglyceride (20-50)
Side Effects
Myopathy, increased liver enzymes Headache, GI distress Flushing, Hyperglycemia, Hyperuricemia, GI distress, hepatotoxicity Dyspepsia, gallstones, myopathy
Fibric Acids
LDL (5-20), HDL (10-20) Triglyceride (20-50) LDL HDL No change in triglycerides
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Case # 1
A 55-year-old woman without symptoms of CAD seeks assessment and advice for routine health maintenance. Her blood pressure is 135/85 mm Hg. She does not smoke or have diabetes and has been postmenopausal for 3 years. Her BMI is 24. Lipoprotein analysis shows a total cholesterol level of 240 mg/dL, an HDL level of 55 mg/dL, a triglyceride level of 85 mg/dL and a LDL level is 180 mg/dL. The patient has no family history of premature CAD.
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Case # 1 (cont.)
What is the goal LDL in this woman? What would you do if exercise/diet change do not improve cholesterol after 3 months? How would your management change if she complained of claudication with walking?
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Case # 2
A 40- year-old man without significant past medical history comes in for a routine annual exam. He has no complaints but is worried because his father had a heart attack at the age of 45. He is a current smoker and has a 23-pack year history of tobacco use. A fasting lipid panel reveals a LDL 170 mg/dL and an HDL of 35 mg/dL. Serum Triglycerides were 140 mg/dL. Serum chemistries including liver panel are all normal.
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Case # 2 (cont.)
What is this patients goal LDL? Would you start medication, and if so, what?
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Case # 3
A 65 year-old woman with medical history of Type II diabetes, obesity, and hypertension comes to your office for the first time. She has been told her cholesterol was elevated in the past and states that she has been following a low cholesterol diet for the past 6 months after seeing a dietician. She had a normal exercise stress test last year prior to knee replacement surgery and has never had symptoms of CHD. A fasting lipid profile was performed and revealed a LDL 130, HDL 30 and a total triglyceride of 300. Her Hgba1c is 6.5%.
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Case # 3 (cont.)
What is this patients goal LDL? What medication would you consider starting in this patient? What labs would you want to monitor in this patient?
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HYPERLIPIDEMIA
Brian V. Reamy, MD, Colonel, USAF, MC Chair Department of Family Medicine Uniformed Services University
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Why Bother?
Optimum treatment of lipids helps in the primary & secondary prevention of ASCVD; still our nations #1 killer
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Why Bother?
ASCVD has been #1 cause of death every year since 1900 with exception of 1918. 50% of CVD diagnoses and 15% of CVD deaths are in patients < 65 years of age Many young adults have 2 or more risk factors that go unrecognized and untreated.
NCEP/ATP III
Step 2: Identify if patient has CAD or equivalent (PAD, DM, AAA, Carotid) Step 3: Risk factor assessment (HTN, FHx, Tob, Age & Sex, HDL<40 or >60) Step 4: If 2 or more risk factors; do Framingham 10-yr risk assessment.
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0 1
HDL = 43
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0 1 0
4
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0 1 0
4
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CHD/10yr <100mg/dl risk>20% (high) 2+RF or <130mg/dl 10yr<20% (Medium) 0-1 risk <160mg/dl factors (low)
>130mg/dl
>160mg/dl
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Statin Pearls
Elevated transaminases on statins; (unless reaching 3x normal), are not a reason to stop the statin they are are a reason to watch closely. Statin side effects are often agent specific, not always class specific. Unexplained myalgias may occur on statins without CK elevation. Try a different statin.
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Statin Pearls
Rhabdomyolysis is uncommon unless CK is elevated to 10 x normal. Usually occurs in patients with multiple co-morbidities. Unless you enjoy driving yourself nuts; do not check CK serially in patients on statins. Remember vigorous yard work will bump your CK! Some think a baseline CK may be helpful. But what about the PROVE-IT study? (NEJM 8 April 2004)
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PROVE-IT Trial
Designed to PROVE that 80mg atorvastatin was no better than 40 mg pravastatin in secondary prevention. But, atorvastatin was superior as early as 30 days of therapy. In just 24 mths the atorvastatin group (meanLDL=62) had 16% less of all CV events. 28% less mortality than pravastatin group (meanLDL=95)
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PROVE-IT Trial
WOW! Evidence from mammalian species had shown that atherogenesis stops & reverses at an LDL <80 now some clinical outcome data.
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LDL
TLC
DRUGS
<70mg/dl >100mg/dl >100mg/dl or <100mg Optional <100mg/dl >130mg/dl >130mg/dl or 100-130 Optional <130mg/dl >130mg/dl >160mg/dl <160mg/dl >160mg/dl >190mg/dl
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TNT - Results
Side Effects: increased LFTs in 0.2% of patients on low dose and 1.2% on high dose. No change in rhabdomyolysis risk. Results: Relative risk reduction of 22% and absolute risk reduction of 2.2% in major cardiovascular events for group with LDL <80 versus group with LDL=101. More evidence to lower our LDL goals
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CASES
All real cases. No perfect answers. All present real Family Practice dilemmas. Will use the evidence to help formulate a best answer. Use cases to convey cutting edge info.
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EBCT (coronary Ca++ score) Lp (a) lipoprotein, Apo B, LDL particle size Homocysteine Plasma Adiponectin
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EBCT
Like with hs-CRP, it is not very useful in low risk or very high risk patients. It significantly correlates w/ cheaper hs-CRP. Best used in intermediate risk folks where it might change treatment approach. In patients w/ intermediate risk an EBCT score >80 has a sensitivity of 85% and a specificity of 75% for the risk of events.
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Homocysteine
High plasma homocysteine may be directly related to atherosclerosis development. Homocysteine may enhance inflammation & thrombosis. There may be no causal association between elevated homocysteine and CV disease risk. New Evidence!!
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Homocysteine
NEJM; 13 April 2006; 2 studies re: homocysteine lowering #1: Secondary prevention: 5522 patients: placebo vs 2,5mg Folate+B6+B12: did not reduce the risk of cardiovascular event, more pts in Tx had unstable angina. #2: 3749 pts post-MI: treatment with Bvitamins did not lower risk of recurrent CV disease. A harmful effect of B-vitamin Tx was suggested.
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Summary
8 Points to make you strong 1) 1 & 2 prevention of ASCVD are possible! 2) NCEP/ATP III at www.nhlbi.nih.gov is useful. 3) The key step is risk assessment & then tailoring treatment to individual risk.
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Summary 8 Points
3) Better medication options are a help: Ezetimibe, Advicor, new statins and a cleaner understanding of statin side effects 4)Attack the metabolic syndrome!! A multi-modal treatment plan is best. 5) Dont ignore a chance for prevention because your patient is >70 or <35.
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Summary 8 Points
6) hs-CRP is a powerful new tool to predict risk; especially in those at intermediate risk. But, we need prospective proof that lowering it will help reduce ASCVD endpoints. 7) Try to get to goal; anticipate new ATP-IV guidelines.
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